Diane Van Horn



Sweating is a natural process for all animals.  Broadly speaking, we sweat so that our brains do not overheat.  The brain can easily overheat if the temperature rises too high because it consumes a very large amount (twenty percent) of our metabolic energy.  The brain and temperature relationship is extremely sensitive because it has been studied that brain damage is apparent if the brain temperature is raised to 106 degrees Fahrenheit.  Therefore, in order for the brain to not reach this temperature, there must be a system that moderates the temperature—this cooling system is commonly referred to as sweating.  When humans sweat, the surface of their skin is cooled, and the skin is then able to cool the blood headed to the brain.  The sweat glands are in charge of carrying out this important system.  There are two components to the sweat glands:  the apocrine glands and the eccrine glands.  The apocrine glands contribute the odor component to sweat and are associated with hair follicles, and the eccrine glands are the actual glands responsible for the secretion of sweat on the skin to lower the body temperature.  (  Dr. Richard G. Glogau explained that:  “Eccrine sweat evaporates on the surface of the skin and effects a transfer of heat, primarily by direct conduction from the vascular supply to the skin.  Sweating can reach volumes measured in liters per hour,” (1998, p.817).  Between two and four million of these glands are found deep in the skin of the palms of hands, in the soles of feet and under the axillary skin. (Glogau, 1998)  These glands secrete a very dilute solution of urea and lactic acid (Odderson, 1998).







Hyperhydrosis is the medical term given to the condition commonly referred to as excessive sweating.  It is necessary for our bodies to sweat, and the Sympathetic Nervous System is in charge of this secretion.  However, one out of every one hundred people suffers from the hyper-activity of this specific nervous system and is said to have the miserable condition known as hyperhydrosis.  Hyperhydrosis can be found in the palms of the hands (palmar hyperhydrosis is the most prevalent of all types) (, on the bottom of the feet, on the face, on the trunk, and in the armpits where the axillary glands are located.  As for a cause, it is not yet known why the nerve stimulation is greater than average in some people (people with hyperhydrosis).  However, in Richard G. Glogau, MD’s study he refers to “an unusual hybrid sweat gland with both eccrine and apocrine elements…which is found in patients with axillary hyperhydrosis, and which is capable of a secretory rate of 10-fold higher than normal eccrine glands,” (1998, p.817).  It is a horrible condition that causes much embarrassment (sweating through and ruining clothes and not being able to lift arms) and much discomfort.  For example, a man named Brandon Burg suffered from hyperhydrosis and would sweat through his shirt in fifteen minutes.  He confesses, “I had to wear Kotex under my arms.  That was the last straw.” (  Research has provided us with a genetic link with abundant stimulation. (  Generally, the condition begins at a young age and will most likely persist for the duration of one’s life.  (  Medically speaking, there is a high level of “cholinergic nerve stimulation of the eccrine sweat glands” ( in the people who suffer from hyperhydrosis. 




There are several options that attempt to treat axillary hyperhydrosis; some of these methods of approach have proven more successful than others.  The first step usually taken is to try a prescribed topical antiperspirant.  The powerful chemical found in these prescriptions is aluminum chloride, usually between 20-25 percent in an alcohol solution.  The aluminum chloride prevents the sweat from escaping the pores (  If the case of hyperhydrosis is heavier than light, the antiperspirant may very well not be effective.  There are additional options yet they all come with drawbacks.  (


One of these options that is not extremely convenient for problems in the axillary area is to use a battery-powered electric current under the arms in twenty minute intervals every few days, gradually increasing the time between intervals to every-other week.  This procedure is referred to as “iontophoresis.” 


Glogau asserts “oral anticholinergic drugs such as glycopyrrolate” (1998, p.817) have been tried by dermatologists to cure hyperhydrosis, yet they have not proven successful.  And although psychotherapy may be recommended, it will not usually be an aid to treating primary hyperhydrosis because it has been proven that it is not a psychological disorder.  However, secondary hyperhydrosis may be treated successfully by psychotherapy.  Primary hyperhydrosis is different from secondary hyperhydrosis in that there is not another disorder linked to hyperhydrosis.  Secondary hyperhydrosis is a side effect of another disorder.  “Secondary hyperhidrosis can be associated with obesity, menopause, drug use (antidepressants), endocrine disorders (htpoglycemia, hyperthyroidism, pheochromocytoma), and neurologic conditions involving autonomic dysregulation…” (1998, p.1237).  “Alternative therapy including homoeopathy, massage, acupuncture and phytotherapeutic drugs” ( have been used to experiment with many sufferers, yet these remedies have not proven successful.  (


There are a few surgical options if the above treatments have not alleviated the excess sweating.


One option is the permanent removal of the sweat glands, and the second is a procedure called sympathectomy.  The sweat glands are removed by scraping out the underarm’s skin.  “The principle of sympathectomy is to interrupt the nerve tracks and nodes (ganglia) which transmit the signals to the sweat glands,” (  A tube is placed inside of the neck to destruct all of the nerve fibers that are connected to the axillary sweat glands.  The dangers of this treatment are numerous:  the patient is out under anesthesia, there could be damage to other nerves in the neck resulting in paralysis, and there could be “permanent dilation of the pupil of the eye as a reflex injury,” (  This process can also cause pneumothorax which is when air or gas is found in a pleural (lung cover) cavity, Horner’s syndrome, and compensatory sweating in other areas of the body occurs in sixty-five to ninety percent of patients, according to Heckmann, Breit, Ceballos-Baumann, Schaller, and Plewig (1999).  Another drawback to this procedure is the gustatory sweating that follows in twenty-eight percent of patients, (  


The last surgical option is the most superficial yet is not as reliable as the other procedures to cure the problem of excessive sweating.  It does not always have great results because the skin of the underarm is scraped on the surface (very superficially) with “liposuction cannulae to remove the sweat glands,” (    


Presently, the final option for hyperhydrosis is that of botox injections.  The term “botox” comes from a group of related toxins produced by Clostridium botulinum.  Clostridium botulinum is a certain bacteria.  Botox is so dangerous that United Nations “inspectors have been searching for hidden stockpiles of this chemical inside Iraq,” (  This toxin is one of the most lethal poisons known, interfering with the effect of the transmitter substance acethylcholine at the synapses (the contact point of a nerve ending with another nerve cell or a muscle),” (  If acethylcholine is not released, the sweat glands will not be stimulated, and if there is no stimulation, the glands cannot secrete the bodily salts and water, which we refer to as sweat.  (  “Botulinum toxin binds to presynaptic nerve membranes and then inhibits release of acetyl choline by disrupting the Ca+2 dependent Ka+ evoked release mechaism,” (  (The injections are expected to give the patients about six months of dryness—sweat free!  Because the toxin “paralyzes” and no sweating occurs in the underarm area for about six months, many patients are worried that other parts of their body will start perspiring excessively because of the decrease in perspiring in the defined area (underarm).  This, however, should not be a concern because “the effects of Botox are strictly focal.  Since only small surface areas are treated the rest of the skin on the arms, legs, torso, and face sweat as before,” (





The history behind botox is very intriguing.  Van Ermengem in 1897 made a significant connection between bolulism and the toxin made by Clostridium botulinum, “an anaerobic gram-positive rod that is commonly found in soil,” described by Ib R. Odderson (1998, p.351).  In 1949 scientists discovered that BTX (botox) “blocks neuromuscular transmission” and then it was experimented in non-human primates, and then humans later in 1981 to treat strabismus.  Strabismus is a disorder concerning the muscles of the eyes in which the eyes cannot be focused on the same thing at the same time.        Botox has been used in other medical circumstances such as “stroke, cerebral palsy, [and] multiple sclerosis,” (  The toxin was first approved to paralyze the nerves in certain hyperactive muscles that were spasmic.  (  There are seven forms of the toxin produced by Clostridium botulinum bacteria; they are referred to as Botox A-G.  The only form that has been approved by the FDA for clinical use is form A.  However, as said before, Botox A has not yet been approved for hyperhydrosis treatment.  There are two brands of the toxin that are currently on the market.  These two brands, Dysport and Botox, have different dosage equivalents, so it is important not to use their names or respective dosages interchangeably.  One unit of Botox equals between three and five units of Dysport.  (Heckmann et al., 1999)  (  Botox definitely does its job well, and it improves the daily lives of many sufferers!




The sweat glands are located between the dermis and the dermis fat/tissue.  The placement of the injections is very sensitive because if injected too deeply it goes into the fat and misses the nerve endings, yet if injected too closely to the surface of the skin, the toxin may not reach the nerve endings to blockade them. 


Doctors should make sure that they are injecting a hyperhydrotic area by performing an iodine test:  place the iodine on the area of the skin, “and then dust it lightly with corn starch powder…The perspiration combines the iodine and glucose in the starch and turns instantly black,” (  If injected properly, the skin should swell and a bump should form similar to one that forms on the skin after a tuberculin test.




Hyperhydrosis patients should be aware that “repeat” doses should not exceed two hundred units of botox at one time because antibodies will be created in the body, and these antibodies will cancel the effect of the toxin.  This said, the smallest dose of botox that proves effective should be given, no more than what is needed  (  Another measure to take so antibodies are not formed is to be careful how great the time interval between injections is:  the next injection should not be less than three months after the patient’s previous injection (  Patients should also be conscious of the price of the injections and know that they are usually not covered by insurance companies.  This is because botox has not yet been approved by the FDA for the treatment of hyperhydrosis and because of the cost of the toxin itself—it is extremely high.  Roughly speaking, each session of injections will be around one thousand to twelve hundred dollars because between one hundred and one hundred and twenty units of botox are generally used, and the cost is about ten dollars per unit.  ( 




The botox should be kept in a freezer until it is used and is “dilated to desired concentration.”  Botox is injected into the axillary sweat glands and surrounding muscle like local anesthetics are fed into the body, via a teflon-coated EMG needle (twenty-three gauge to twenty-six gauge) and syringe. (  Usually each underarm will take twelve to fifteen injections.  This procedure is very safe because there is no anesthesia.  There are, in most cases no side effects that the patient experiences following the procedure, yet exercise is not encouraged for a few hours.  However, the patient may participate in any routine activity, i.e. driving, work, walking, and mental thought.  According to Heckmann et al. (1999) “none of the patients noticed muscular weakness or any other neurologic deficit.  Four patients felt a temporary stinging during the first day after treatment, however, which subsided without further intervention” (1999, p.989).  Odderson (1998) mentions a microscopic study of the tissue where the eccrine glands are located in his review.  He writes:  “Histologic examination of an axillary skin biopsy before and after botulinum toxin treatment did not reveal any differences in sweat gland morphology or innervation.” (1998, p.1239)  By morphology, he means the shape, form, and structure of the glands and by innervation he means the stimulation of nerves.


The only physical evidence of the injections that a patient may see are little bruises in the area where the injections were given, but they diminish after a few days.  However, bruises are not found on all patients.  Every so often, one may feel weak and spent after the injections but these complaints are very rare, and the feelings are usually gone in less than four days (  Some patients may also discover that certain areas are sweating in the underarm.  This means that the doctor missed a small spot.  This problem can be resolved by going back to the doctor for a touch-up visit to nail the areas that he/she missed.  The patient should not worry because these are not considered re-injections—they were just spots that the doctor originally missed. 


The botox does not take effect when the patient leaves the doctor’s office; it is not immediate.  The research claims that ninety-five percent of the sweating will decrease within the first forty-eight hours and that it will take one full week to reach its full effect.  Once the botox has reached its full effect, it should last for between five and six months.  (  However, another report claims slightly different observations:  the effect is onset twenty-four to seventy-two hours after injection, the peak effect is four to six weeks, and the average duration of its effect is between three and four months. (  Because the reports differ slightly, it would be feasible to expect somewhere in between the two.  The botox molecule is a:

“light and heavy chain linked by a disulfide bond (heavy chain is responsible for binding; light chain is intracellular toxic moiety).  Like tetanus toxin, BTX is a zinc endopiptidase.  Its seven serotypes differ in their cellular targets as well as their potency and duration of action.  The type A toxin selectively cleaves a protein called SNAP-25.  This protein is one of several involved in the fusion of vesicles containing neurotransmitters within the nerve terminal membrane.  The complexity of this mechanism may account for the relatively slow onset of the effect of botulinum toxin: 2-72 hours…Axon sprouting terminates the clinical effect usually in 2-6 months.” (




Although many dermatologists are yet to offer botox injections to their patients who suffer from hyperhydrosis, the physicians that are aware of its effect find the discovery very exciting and promising.  “This is probably the biggest development in the history of sweating for people that have a major abnormal sweating problem.  I’m excited about it.  I think this is a major breakthrough,” reports Dr. Darrell Rigel, president-elect of the American Academy of Dermatology (  Although the Food and Drug Administration (FDA) has not approved botox for hyperhydrosis injections, it has approved botox for “treatment of muscle spasms.”  Therefore, since botox has not officially been approved for treating cases of excessive sweating, it is said to be an “off-label” treatment.  (  The information presented on the internet seems to be credible and the dermatologists and cosmetic surgeons appear to think highly of the procedure and the overall treatment.




There have been several convincing studies on botox and its effects on patients with hyperhydrosis.  Glogau performed a study in 1998 in which he concluded that “offset against the social stigma, emotional stress, and costs associated with clothing wear, repair, and cleaning, Botox appears to offer a significant and elegant therapeutic advance in the treatment of axillary hyperhydrosis,” (1998, p.819).  He took eight females and four males ranging in age from twenty-five to forty-five years old.  Each patient had to be tested prior to the procedure to see if he was in fact a fair candidate for the study.  Each patient rested in “cool ambient temperatures and minimal psychic stress to effectively soak through a shirt or blouse in less than 5 minutes despite prior drying of the axillary vaults by wiping,” (1998, p.818).  The botox was injected starting on the edge of the hair-bearing skin and working its way inward in a spiral pattern to the center of the area.  Fifty mU of Botox was used in a solution of sterile saline in each arm.  The only immediate side effect was “minor pinpoint hemorrhage at the site of entry of the needle,” (1998, p.818).  Patients had follow-up visits after one week and one month had passed since the injections.  All twelve candidates reported that most of their sweating had disappeared within forty-eight hours after the Botox entered their bodies.  Statistics wise, the earliest recurrence of excessive sweating was after four months, the longest “dry” time was seven months, and the average “dry” time was 5.2 months.  The study concluded with the reinjection of Botox and a follow-up period of five additional months for five out of the twelve patients.  The study proved that reinjections of Botox keep the sufferers drier for a longer span of time than the initial injection (the first sign of hyperhydrosis came five months after the reinjections).  (Glogau, 1998)


Heckmann et al. (1999) performed an open clinical trial similar to that of Glogau’s.    Twelve patients were selected by how much they sweat:  they each had to secrete greater than one hundred milligrams per axilla per minute.  This measurement was performed by gravimetry:  filter paper was massed before being inserted under the arm and again after being soaked from being under the arm for exactly a minute.  This measures the rate of secretion per minute.  Also, photographs were taken of the stains caused by the sweating, and it was seen that most of the stains were larger than fifteen centimeters in diameter.  (Heckmann et al., 1999)  More specific than the other study, this study only injected one of the axilla so that the other axilla would serve as the control.  However, after exactly two weeks had passed since the first injection, the other axilla was injected.  In between this period though, after three days and after a week gravimetry was used to compare the injected axilla versus the non-injected axilla.  After both axillae were injected, the patients checked-in every three months to be examined.  In line with the other study, all of the twelve patients reported a huge decrease in sweating between forty-eight and seventy-two hours after leaving the doctor’s office.  This quantitative observation is very interesting:  “sweat rates ranged from 150 to 890 mg/min, revealing considerable interindividual variations before treatment.  Seven days after treatment, however, sweat rates had dropped to below 50 mg/min consistently in each patient,” (1999, p.989).  The patients’ evaluations of the procedure were very convincing.  Out of four choices, being “completely satisfied,” “almost completely satisfied,” “partly satisfied,” and “not satisfied,” ten sufferers claimed that they were “completely satisfied” and only two said that they were “almost completely satisfied.”  Heckmann et al. reports:  “The longest symptom-free interval recorded up to the present was 12 months [7 patients] and 9 months [3 patients].  The two patients with the highest initial sweat rates…reported recurrence of sweating between 3 and 6 months after BT-A injection,” (1999, p.989). 


Ib R. Odderson, MD, PhD (1998) did a simple, very limited study between two brothers who had both suffered from hyperhydrosis for years.  One was a thirty-nine year old hairdresser and the other was thirty-six and an aircraft mechanic.  “They received bilateral axillary injections with 100 units of botulinum toxin type A, and within 5 days reported cessation of excessive sweating.  Quantitative measurements before and 2 to 4 weeks after the injections demonstrated an average reduction of 71% and 76% in axillary sweating during rest.  A 96% reduction was seen in [the hairdresser] during mental stress,” (1998, p.350).  The hairdresser noticed that the sweating started up again after about eleven weeks of being dry, whereas his younger brother reported that the sweating had returned approximately eight weeks after the injections.  In the discussion, Odderson points to evidence that the toxin successfully blocks sweating by comparing the sweat rate during rest and during mental stress:  they are extremely similar (1.6 and 1.4 mL/min m-sqrd., respectively).  Here is an interesting comparison:  “The subject’s average resting sweat rate after the injections was similar to the rate observed for men resting in the shade in the desert, whereas before the injections his average resting sweat rate was 150% of that of men walking in the desert sun,” (1998, p.351).


Odderson (1998) also wanted to explore what botulinum toxin injections would do to healthy subjects.  He wrote a review paper on males that were injected in each axilla with 50 U, 30 U, and 20 U, and the results were complete anhidrosis for eight months, sweating reduction that lasted for six months, and no effect on the amount or frequency of sweat secretion, respectively.  Therefore, Odderson proved that “axillary injections in healthy subjects showed a dose-related effect and time response,” (1998, p.1238).  In his review he discusses two studies that were done on people that were suffering from hyperhydrosis.  The first study he refers to consisted of seven patients each receiving 2-cm apart injections in the axillary region.  The dilution of the toxin was 100U/ml, and between 28 and 48 U’s were placed in each axilla.  The result:  “Hyperhidrosis remained absent in all patients after an observation period of 1 or 8 months,” (1998, p.1239).  A larger dose of 50U per axilla was given to twelve suffering patients in another study, but these injections were given more closely to each other—1.0-1.5 cm apart.  The presence of sweating was calculated subjectively to arrive on an average of 5.2 (range 4-7) months following the injections.  Odderson obviously found all of the studies that he refers to very encouraging.  Another study that he mentions concludes that in one study, the amount of sweat secreted in one minute decreased by eighty-five percent two weeks after the injections—amazing!  In his discussion he finishes by saying:  “A total of 50U of botulinum toxin per axilla is adequate to reduce sweating by 70-80% or clinically abolish sweating in healthy volunteers and patients with hyperhidrosis.” (1998, p.1239) 


Alberto Goldman, M.D. (2000) designed another study on the treatment of axillary and palmar hyperhidrosis with botulinum toxin.  His results comply with the previous mentioned studies’ findings.  A large group of patients, two hundred and forty-three (69.9 f : 30.1 m), suffering from severe hyperhydrosis were gathered and received injections of the toxin.  The age of the patients ranged from seventeen to fifty-four years old, and eight of the patients had previously had axilla surgery and two had sympathectomy.  But, in all of these cases, there was either partial or complete relapse of the condition.  From the results of the injections and the absence of sweat, Goldman concluded that the effects of the toxin lasted “from 5 to 14 months.  Ninety-three patients (38%) were given drug reapplication after the sweating returned.  All patients reported that symptom return was less intense.  The drug amount required as of the second treatment was approximately 20% lower and improvement symptoms often lasted longer, probably due to lower neurimotor plate neoformation,” (2000, p.281).


P. Schnider et al. (1999) conducted a randomized, double-blind, placebo-controlled trial of botulinum A toxin for severe axillary hyperhidrosis that was approved by the Ethics Committee of the Medical Faculty of the University of Vienna.  Thirteen people were part of the study:  there were nine females and four males.  Like Heckmann et al. (1999), this study left one axilla as the control by only injecting one axilla with 200U of Dysport and the other axilla was injected with saline.  Both kinds of injections looked the same on the skin so the placebo and active sides could not be distinguished.  Digitized ninhydrin-stained sheets were used to objectively measure the amount of sweat at certain time intervals following the injections.  “Three weeks after treatment, the mean difference in ninhydrin staining between botulinum-treated and placebo-treated axillae was –34.5% (P<0.001), after 8 weeks –36.9% (P<0.001) and after 13 weeks –28.4% (P<0.001),” (1999, p.677).  Therefore, from these statistics, it is concluded that the height of the botox’s effect was somewhere around eight weeks after the injections. (P. Schnider et al., 1999)


Markus Naumann, MD et al. (1998) designed a before and after trial, supported by the Department of Neurology, University of Walzburg, and Allergan, over a time span of four months.  Ten females and one male, with a mean age of 30.5 years, that have been suffering from hyperhydrosis for an average of 10.8 years, were treated with botulinum toxin A.  Out of the eleven patients, seven had the condition only present in the axillary region, two patients only in the palmar area, and axillary and palmar in one patient, and palmar and plantar in one patient.  Iodine-starch tests were given to each patient prior to the toxin injections and also two, four, twelve, sixteen, and twenty weeks proceeding the procedure.  In this test an iodine solution is spread over the affected area, and then “fine rice or potato starch powder is applied.  Sweat causes the mixture to turn dark blue,” (1998, p.301).  Similar to other studies discussed above, the effects of the injections were measured gravimetrically in ten patients.  These measurements were taken before the procedure and two weeks following.  The results of this treatment were very encouraging because the injections “abolished clinically disturbing hyperhidrosis in all patients,” (1998, p.302).  Statistic wise, the trial was successful:  after a mean of 2.8 +/- 0.7 days the patients started to notice a difference in their sweating levels, there was no sweating after a mean of 5.4 +/- 1.4 days, and lastly, quantified from the Minor test, it was observed that the surface area of hyperhydrosis activity decreased from 46.4 +/- 9.8 squared centimeters before the injections to hugely reduced or no sweating two weeks following.  Another noteworthy finding:  “there was no evidence of compensatory hyperhydrosis in other areas after treatment,” (1998, p.302).  The most comforting discovery is that when the hyperhydrosis resurfaces, injections can be given again successfully.  “Within the follow-up period of up to 20 weeks (range, 12-20 weeks), no clinical hyperhidrosis could be discovered in 8 of 11 patients.  However, 16 weeks after injection, small areas of clinically inapparent restored axillary sweating were observed with the Minor test in 3 patients, all of whom were successfully reinjected 4 weeks later,” (1998, p.303).  The difference in function of the apocrine and eccrine sweat glands was also highlighted in this trial.  The interesting observation was made that although the toxic injections paralyzed the nerves from releasing sweat, the odor component of sweat was still present.  This is because the glands have different transmitters being released to carry out the actions; the adrenergic sympathetic nerve fibers “supply” the apocrine glands, and these fibers are not affected at all by botulinum toxin.



Glogau, M.D.(1998).  Botulinum A Neurotoxin for Axillary Hyperhidrosis. 

Dermatologic Surgery, 24, 817-819.


Goldman, A. (2000).  Treatment of Axillary and Palmar Hyperhidrosis with Botulinum

Toxin.  Aesthetic Plastic Surgery, 24, 280-2.


Heckmann, M., Breit, S., Ceballos-Baumann, A., Schaller, M., & Plewig, G. (1999). 

Side-controlled Intradermal Injection of Botulinum Toxin A in Recalcitrant

Axillary Hyperhidrosis.  J Am Acad Dermatol, 41, 987-90.


Naumann, M. et al. (1998).  Focal Hyperhidrosis:  Effective Treatment With

Intracutaneous Botulinum Toxin.  Archives of Dermatology, 134, 301-4.


Odderson, Ib R. (1998).  Axillary Hyperhidrosis:  Treatment With Botulinum Toxin A. 

Arch Phys Med Rehabil, 79, 350-2.


Odderson, I.R. (1998).  Hyperhidrosis Treated by Botulinum A Exotoxin.  Dermatol

Surg, 24, 1237-41.


Schnider, P. et al. (1999).  A Randomized, Double-blind, Placebo-Controlled trial of

Botulinum A Toxin for Severe Axillary Hyperhidrosis.  British Journal of

Dermatology, 140, 677-80.




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